The purpose of this study was to determine whether dietary (n-3) fatty acids would affect mammary tumor growth and metastasis. Weanling female BALB/c mice were fed diets that contained 10% corn oil (CO), linseed oil (LO) or a fish oil-corn oil mix (FO) for 3-8 wk prior to receiving subcutaneous injections of one of two syngeneic mammary tumor cell types (410 and 410.4). Tumor growth was assessed by monitoring mean tumor diameter and tumor weight upon removal. Feeding LO, but not FO, reduced the growth (p less than 0.05) of 410.4 mammary tumors compared with growth in those fed CO. Metastasis data paralleled the tumor growth rate. Feeding LO and FO enhanced (p less than 0.005) incorporation of (n-3) fatty acids into tumors. Tumor prostaglandin E (PGE) production was reduced (p less than 0.005) by LO and FO, compared with CO. FO feeding reduced 410.4 tumor PGE synthesis more (p less than 0.05) than LO feeding, yet tumor growth was only inhibited by LO. These data suggest an inhibitory effect of dietary linolenic acid [i.e., 18:3 (n-3)] on mammary tumor growth and metastasis. However, this effect did not directly correlate with diet-induced changes in PGE synthesis.

Feeding of purified diets containing fish oil without added antioxidant leads to rapid autoxidation of the oil and the possibility of artifactual results due to the feeding of autoxidation products. Purified diets containing menhaden oil without any added antioxidant deteriorate quickly. Peroxide value of the diet is elevated 5- to 6-fold within 24 h and 12-fold within 48 h when exposed to air at room temperature. Addition of 0.02% t-butylhydroquinone to the fish oil prevents this deterioration for at least 72 h. Determination of fatty acid composition is not a sensitive indicator of diet integrity. Supplementation of fish oil diets with vitamin E to help protect against in vivo peroxidation is discussed.

No abstract

Semipurified diets containing ratios of alpha-linolenic acid (18:3 omega 3) to linoleic acid (18:2 omega 6) of 1/32, 1/7, 1/1, and 3.5/1 in the form of corn oil, soybean oil, soybean/linseed oil mix and linseed oil were fed to rats for 2 months. The first 3 diets were fed to another group of rats for 4 months and to a group through the second generation. Fatty acid analysis of liver and spleen ethanolamine glycerophosphatide revealed that, as the level of 18:3 omega 3 in the diet increased, the elongated, desaturated metabolites of the omega 6 series decreased and the omega 3 series increased. Noteworthy was the depression in the amount of the precursor of the 2-series prostaglandins (PG) as the omega 3 levels increased. Synthesis of PG by liver of rats fed 2 or 4 months markedly decreased, but at 2 months in thymus and spleen, it showed a trend toward decreasing only. Brain slices showed no decrease in PGF2 alpha synthesis after 4 months, but did decrease significantly after feeding the diets to the second generation. Synthesis of PGE2 by spleen homogenate from the second generation also significantly decreased. The replacement of omega 6 series fatty acids by omega 3 series is explained by the effective competition of 18:3 omega 3 over 18:2 omega 6 for the delta 6 desaturase. Depressions in PG synthesis by high dietary 18:3 omega 3 is explained by the competitive inhibition of the PG synthetase complex by 20:5 omega 3 as well as by the decreased levels of 20:4 omega 6.

Sprague-Dawley rats were fed diets including 10% corn oil (CO), 10% hydrogenated coconut oil (HCO) or 10% linseed oil (LO), and immune cell populations isolated from peripheral blood and spleen were examined for alterations in prostaglandin E (PGE) synthesizing capacity and mitogen-induced blastogenesis. Culture conditions were optimized by incubating the cells in serum obtained from animals fed the same diet. The fatty acid profiles of these sera reflected the composition of the dietary fat ingested. Both the LO and HCO diet treatments resulted in significantly lower PG-synthesizing capacity by both unstimulated and phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells or splenocytes when compared to the CO group. Mitogen-induced [3H]thymidine uptake by splenocytes from rats fed the HCO diet was twofold higher than responses observed in cells from animals fed the LO or CO diets. The results suggest that mitogenesis is not influenced by the diet-induced change in immune cell PGE2 synthesizing capacity. Enhanced [3H]thymidine incorporation was associated with a greater degree of saturation of dietary fat.